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Antiandrogens as environmental endocrine disruptors

W R Kelce1, L E Gray, E M Wilson

  • 1Reproductive Toxicology Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA. wkelce@med.unc.edu

Reproduction, Fertility, and Development
|September 4, 1998
PubMed
Summary

Environmental chemicals like vinclozolin disrupt male reproductive development by blocking androgen receptor activity. This research explores the molecular mechanisms behind this antiandrogen toxicity.

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Environmental science & technology·2012

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Environmental Toxicology

Background:

  • Steroid hormone receptors are critical for embryonic development and sex differentiation.
  • Hormonal disruptions during development can have severe and lasting consequences.
  • Environmental chemicals can interfere with essential hormonal signaling pathways.

Purpose of the Study:

  • To investigate the molecular mechanisms by which environmental chemicals disrupt male reproductive development.
  • To understand how antiandrogens inhibit androgen receptor-mediated gene transcription.
  • To elucidate the basis of environmental antiandrogen toxicity.

Main Methods:

  • Utilized a variety of in vitro and in vivo experimental approaches.
  • Analyzed the binding affinity of environmental chemicals to the androgen receptor.

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  • Assessed the antagonistic effects on androgen-dependent gene expression.

    • Main Results:

    • Environmental chemicals, including vinclozolin and DDT metabolites, were identified as inhibitors of androgen receptor function.
    • These chemicals bind to the androgen receptor with moderate affinity.
    • They act as antagonists, preventing the transcription of androgen-dependent genes.

    Conclusions:

    • Environmental antiandrogens disrupt male reproductive development by antagonizing the androgen receptor.
    • Understanding these molecular interactions is crucial for assessing developmental risks.
    • Further research is needed to fully characterize the impact of environmental endocrine disruptors.